2016
Increased susceptibility of Cftr−/− mice to LPS-induced lung remodeling
Bruscia E, Zhang P, Barone C, Scholte BJ, Homer R, Krause D, Egan ME. Increased susceptibility of Cftr−/− mice to LPS-induced lung remodeling. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2016, 310: l711-l719. PMID: 26851259, PMCID: PMC4836110, DOI: 10.1152/ajplung.00284.2015.Peer-Reviewed Original ResearchConceptsLung pathologyCF miceImmune responseWT miceChronic inflammationCystic fibrosisAbnormal immune responseChronic pulmonary infectionPersistent immune responseWild-type littermatesCF mouse modelsPseudomonas aeruginosa lipopolysaccharideCF lung pathologyPulmonary infectionChronic administrationLPS exposurePersistent inflammationLung remodelingWT littermatesLung tissueOverall pathologyMouse modelInflammationChronic exposureBacterial products
2005
Inhibition of the Src and Jak Kinases Protects against Lipopolysaccharide-induced Acute Lung Injury
Severgnini M, Takahashi S, Tu P, Perides G, Homer RJ, Jhung JW, Bhavsar D, Cochran BH, Simon AR. Inhibition of the Src and Jak Kinases Protects against Lipopolysaccharide-induced Acute Lung Injury. American Journal Of Respiratory And Critical Care Medicine 2005, 171: 858-867. PMID: 15665321, DOI: 10.1164/rccm.200407-981oc.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsCapillary Leak SyndromeEnzyme ActivationEnzyme InhibitorsEscherichia coliGene Expression RegulationGene Transfer TechniquesIndolesJanus Kinase 2LipopolysaccharidesLungMiceMice, Inbred BALB CProtein-Tyrosine KinasesProto-Oncogene ProteinsRespiratory Distress SyndromeSignal TransductionSrc-Family KinasesSulfonamidesTranscriptional ActivationTyrphostinsConceptsAcute lung injuryLung injuryCytokine productionLPS challengeSmall molecule inhibitorsLipopolysaccharide-induced acute lung injuryLethal LPS challengeLung cytokine productionSystemic cytokine productionSelective tyrosine kinase inhibitorLung vascular permeabilityMurine lung injuryTyrosine kinase inhibitorsNovel therapeutic agentsMolecule inhibitorsSuppressor of cytokineChemokine productionSystemic inhibitionAirway epitheliumVascular permeabilitySpecific small molecule inhibitorsInjurySrc kinaseTherapeutic agentsKinase inhibitors
2004
Activation of the STAT pathway in acute lung injury
Severgnini M, Takahashi S, Rozo LM, Homer RJ, Kuhn C, Jhung JW, Perides G, Steer M, Hassoun PM, Fanburg BL, Cochran BH, Simon AR. Activation of the STAT pathway in acute lung injury. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2004, 286: l1282-l1292. PMID: 14729509, DOI: 10.1152/ajplung.00349.2003.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsCells, CulturedDisease Models, AnimalDNA-Binding ProteinsHydrochloric AcidInterleukin-6Janus Kinase 2KineticsLipopolysaccharidesLiverLungMaleMiceMice, Inbred BALB CMice, Inbred C57BLMitogen-Activated Protein KinasesOxidation-ReductionPancreatitisProtein-Tyrosine KinasesProto-Oncogene ProteinsRespiratory Distress SyndromeRespiratory MucosaSrc-Family KinasesSTAT3 Transcription FactorTrans-ActivatorsTumor Necrosis Factor-alphaConceptsAcute lung injuryIL-6Lung injuryLPS treatmentDevastating clinical problemGastric acid aspirationIntranasal LPS administrationResident lung cellsSTAT3 activationAcute pancreatitis modelSTAT activationAcid aspirationLPS administrationCytokine responsesInflammatory cellsInflammatory responsePancreatitis modelClinical problemMultiple organsLungLung cellsLPSEndothelial cellsTranscription factorsCritical mediator